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The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes
Platelet-released growth factors (PRGF) and its related clinically used formulations (e.g., Vivostat Platelet-Rich Fibrin (PRF®)) contain a variety of chemokines, cytokines, and growth factors and are therefore used to support healing of chronic, hard-to-heal, or infected wounds. Human beta-defensin...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547724/ https://www.ncbi.nlm.nih.gov/pubmed/28811680 http://dx.doi.org/10.1155/2017/6157491 |
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author | Bayer, Andreas Lammel, Justus Tohidnezhad, Mersedeh Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Cremer, Jochen Jahr, Holger Rademacher, Franziska Gläser, Regine Harder, Jürgen |
author_facet | Bayer, Andreas Lammel, Justus Tohidnezhad, Mersedeh Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Cremer, Jochen Jahr, Holger Rademacher, Franziska Gläser, Regine Harder, Jürgen |
author_sort | Bayer, Andreas |
collection | PubMed |
description | Platelet-released growth factors (PRGF) and its related clinically used formulations (e.g., Vivostat Platelet-Rich Fibrin (PRF®)) contain a variety of chemokines, cytokines, and growth factors and are therefore used to support healing of chronic, hard-to-heal, or infected wounds. Human beta-defensin-3 (hBD-3) is an antimicrobial peptide inducibly expressed in human keratinocytes especially upon wounding. The potent antimicrobial activity of hBD-3 together with its wound closure-promoting activities suggests that hBD-3 may play a crucial role in wound healing. Therefore, we analyzed the influence of PRGF on hBD-3 expression in human primary keratinocytes in vitro. In addition, we investigated the influence of Vivostat PRF on hBD-3 expression in artificially generated human skin wounds in vivo. PRGF treatment of primary keratinocytes induced a significant, concentration- and time-dependent increase in hBD-3 gene expression which was partially mediated by the epidermal growth factor receptor (EGFR). In line with these cell culture data, in vivo experiments revealed an enhanced hBD-3 expression in experimentally produced human wounds after the treatment with Vivostat PRF. Thus, the induction of hBD-3 may contribute to the beneficial effects of thrombocyte concentrate lysates in the treatment of chronic or infected wounds. |
format | Online Article Text |
id | pubmed-5547724 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-55477242017-08-15 The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes Bayer, Andreas Lammel, Justus Tohidnezhad, Mersedeh Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Cremer, Jochen Jahr, Holger Rademacher, Franziska Gläser, Regine Harder, Jürgen Mediators Inflamm Research Article Platelet-released growth factors (PRGF) and its related clinically used formulations (e.g., Vivostat Platelet-Rich Fibrin (PRF®)) contain a variety of chemokines, cytokines, and growth factors and are therefore used to support healing of chronic, hard-to-heal, or infected wounds. Human beta-defensin-3 (hBD-3) is an antimicrobial peptide inducibly expressed in human keratinocytes especially upon wounding. The potent antimicrobial activity of hBD-3 together with its wound closure-promoting activities suggests that hBD-3 may play a crucial role in wound healing. Therefore, we analyzed the influence of PRGF on hBD-3 expression in human primary keratinocytes in vitro. In addition, we investigated the influence of Vivostat PRF on hBD-3 expression in artificially generated human skin wounds in vivo. PRGF treatment of primary keratinocytes induced a significant, concentration- and time-dependent increase in hBD-3 gene expression which was partially mediated by the epidermal growth factor receptor (EGFR). In line with these cell culture data, in vivo experiments revealed an enhanced hBD-3 expression in experimentally produced human wounds after the treatment with Vivostat PRF. Thus, the induction of hBD-3 may contribute to the beneficial effects of thrombocyte concentrate lysates in the treatment of chronic or infected wounds. Hindawi 2017 2017-07-25 /pmc/articles/PMC5547724/ /pubmed/28811680 http://dx.doi.org/10.1155/2017/6157491 Text en Copyright © 2017 Andreas Bayer et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Bayer, Andreas Lammel, Justus Tohidnezhad, Mersedeh Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Cremer, Jochen Jahr, Holger Rademacher, Franziska Gläser, Regine Harder, Jürgen The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes |
title | The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes |
title_full | The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes |
title_fullStr | The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes |
title_full_unstemmed | The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes |
title_short | The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes |
title_sort | antimicrobial peptide human beta-defensin-3 is induced by platelet-released growth factors in primary keratinocytes |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547724/ https://www.ncbi.nlm.nih.gov/pubmed/28811680 http://dx.doi.org/10.1155/2017/6157491 |
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